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Cellular and molecular characterization of type II diabetic bladder dysfunction (865.12)
Author(s) -
Klee Nicole,
Moreland Robert
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.865.12
Subject(s) - carbachol , endocrinology , medicine , type 2 diabetes , streptozotocin , diabetes mellitus , muscarinic acetylcholine receptor , bethanechol , stimulation , downregulation and upregulation , isometric exercise , purinergic receptor , receptor , chemistry , biochemistry , gene
In a rat model of Type II diabetes (T2D), cellular and molecular alterations in muscarinic and purinergic receptor stimulation and associated downstream signaling molecules in bladder smooth muscle was examined over time. T2D was induced in Sprague Dawley rats using the combination of a high fat diet and low dose streptozotocin (HFD/STZ). A 40% HFD was initiated in 14 week old rats; after one month, rats were administered two low doses of STZ (30 mg/kg) one week apart. This model results in obesity, hyperglycemia, insulin resistance, and has been shown to induce diabetic bladder dysfunction (DBD); although this model has rarely been used to characterize DBD or determine mechanistic changes in the regulation of the bladder. DBD is a common complication of T2D, a non‐life threatening complication of diabetes that has a significant negative impact on quality of life. Bladder smooth muscle was isolated and isometric force was recorded in response to the cumulative and non‐cumulative addition of carbachol, bethanechol, ATP, and KCl in both control and HFD/STZ rats. Urodynamic profile, body weight, and glucose measurements were recorded over time pre and post STZ injections. The results of these studies can then be used to determine the efficacy of current and novel therapeutic interventions aimed specifically at the site of dysfunction induced by T2D as well as potential sites of dysfunction affected by aging. Grant Funding Source : NIH DK 85734